A Hemodynamic Model of Pelvic Venous Insufficiency-Induced Prostatic Stasis: A Computational, Falsifiable Framework with Clinical Translation

Benign prostatic hyperplasia (BPH) and chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) are traditionally viewed through the lens of hormonal dysregulation or occult infection. We propose a paradigm shift towards a hemodynamic origin: pelvic venous insufficiency (PVI) leading to chronic prostatic venous stasis. The prostate’s valveless venous drainage (Batson’s and Santorini’s plexuses) creates a hydraulic vulnerability that, when combined with increased intra-abdominal pressure, results in blood pooling, tissue hypoxia, and eventual fibrosis. We formalize this mechanism using a lumped‑parameter Windkessel model, deriving explicit pressure–volume–fibrosis dynamics. A comprehensive parameterization, global sensitivity analysis, and Bayesian calibration against experimental hydroxyproline data are presented, yielding R² = 0.91, p < 0.001. We then simulate a venotonic intervention (reduction of outflow resistance) analogous to the clinical effect of micronized purified flavonoid fraction (Daflon), showing that timely hemodynamic correction can halt and partially reverse fibrosis, reducing fibrotic volume by 45% at day 365. A translational roadmap specifies quantitative diagnostic thresholds (intraprostatic venous pressure >15 mmHg) and incorporates potential synergism with mast‑cell stabilizers. The entire computational framework is open and reproducible, supporting a shift from hormonal to hydraulic rehabilitation in prostatic disease.